APH-2/nicastrin functions in LIN-12/Notch signaling in the Caenorhabditis elegans somatic gonad

被引:44
作者
Levitan, D
Yu, G
Hyslop, PSG
Goutte, C
机构
[1] Schering Plough Res Inst, Kenilworth, NJ 07033 USA
[2] Univ Toronto, Ctr Res Neurodegenerat Dis, Toronto, ON M5S 3H2, Canada
[3] Amherst Coll, Dept Biol, Amherst, MA 01002 USA
基金
美国国家卫生研究院;
关键词
APH-2; LIN-12; Notch; nicastrin; presenilin; C; elegans; Alzheimer's disease;
D O I
10.1006/dbio.2001.0486
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Nicastrin is a recently identified member of high-molecular weight complexes containing presenilin. The Caenorhabditis elegans homolog of nicastrin, aph-2, was shown to be required for GLP-1/Notch signaling in the early embryo. In addition to the maternal-effect embryonic lethal phenotype, aph-2 mutant animals also display an egg-laying defect. We show that this latter defect is related to the SEL-12/presenilin egg-laying defect. We also show that aph-2 and sel-12 genetically interact and cooperate to regulate LIN-12/Notch signaling in the development of the somatic gonad. In addition, aph-2 and lin-12/Notch genetically interact. We illustrate a new role for aph-2 in facilitating lin-12 signaling in the somatic gonad, thus providing evidence that APH-2 is involved in both GLP-1/Notch- and LIN-12/Notch-mediated signaling events. Finally, we demonstrate that nicastrin can partially substitute for aph-2, suggesting a conservation of function between these proteins. (C) 2001 Elsevier Science.
引用
收藏
页码:654 / 661
页数:8
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